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Neuro Endocrinol Lett. 2019 Dec;40(6):289-296.

Neuropeptide Y knockdown in the dorsomedial hypothalamus improved basal and obesity-induced decrease in bone mass density.

Author information

1
Health Management Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China.
2
Departments of Endocrinology and Metabolism, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China.
3
Department of Environmental Health, College of Public Health, Zhengzhou University, Zhengzhou 450052, Henan, China.

Abstract

OBJECTIVE:

Neuropeptide Y (NPY) has been shown to have a prominent role in the control of bone formation through the regulation of osteoblast activity. We aimed to investigate the role of hypothalamus-derived NPY in bone metabolism.

METHODS:

Accordingly, adeno-associated virus (AAV)-mediated RNA interference (RNAi) was utilized to downregulate NPY gene expression in rats fed regular chow (RC) or a high-fat diet (HF). The serum concentrations of glucose, insulin, corticosterone, osteocalcin, insulin-like growth factor (IGF-1), triglycerides (TC), and cholesterol (TG) and fat mass and bone mineral density (BMD) were measured to assess the effect of NPY knockdown on basal and obesity-induced BMD. Forkhead transcription factor (FoxO1) and activating transcription factor 4 (ATF4) were measured to explore the molecular mechanism of the effect of dorsomedial nucleus (DMH) NPY knockdown on bone formation.

RESULTS:

Our results showed that DMH NPY knockdown enhanced basal and the obesity-induced decrease in BMD and osteocalcin and promoted the phosphorylation of FoxO1 and reduced the expression of ATF4.

CONCLUSION:

Our data suggest that DMH NPY knockdown can alter bone metabolism.

PMID:
32200588

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